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• Neonatal respiratory distress syndrome Surfactant deficiency → ↑ surface tension → alveolar collapse ("ground-glass" appearance of lung fields). - Screening tests for fetal lung maturity: lecithin-sphingomyelin (L/S) ratio in amniotic fluid (>2 is healthy; <1.5 predictive of NRDS), foam stability index, surfactant-albumin ratio. Another name for lecithin is phosphatidylcholine.- Persistently low O2 tension → risk of PDA. Risk factors:- Prematurity- Maternal diabetes (due to ↑ fetal insulin)- C-section delivery (↓ release of fetal glucocorticoids; less stressful than vaginal delivery) Complications: PDA, necrotizing enterocolitis Treatment: maternal steroids before birth; exogenous surfactant for infant.- Therapeutic supplemental O2 can result in retinopathy of prematurity, intraventricular hemorrhage, bronchopulmonary dysplasia.
• Methemoglobin - oxidized form of Hb (Ferric, Fe3+) that does not bind O2 as readily, but has ↑ affinity for cyanide - may present with cyanosis and chocolate-colored blood - Induced methemoglobinemia (using nitrates, followed by thiosulfate) may be used to treat cyanide poisoning - can be treated with methylene blue and vitamin C
• Carboxyhemoglobin - Form of Hb bound to CO instead of O2 - Causes ↓ oxygen-binding capacity with left shift in oxygen-hemoglobin dissociation curve- ↓ O2 unloading in tissues - CO bind competitively to Hb and with 200x greater affinity than O2 - Treat with 100% O2 and hyperbaric O2
• Oxygen-hemoglobin dissociation curve Sigmoidal shape due to positive cooperativity (ie, tetrameric Hb molecule can bind 4 O2 molecules and has higher affinity for each subsequent O2 molecule bound). Myoglobin is monomeric and thus does not show positive cooperativity; curve lacks sigmoidal appearance. Shifting the curve to the right → ↓ Hb affinity for O2 (facilitates unloading of O2 to tissue) → ↑ P50 (high PO2 required to maintain 50% saturation).Shifting the curve to the left → ↓ O2 unloading → renal hypoxia → ↑ EPO synthesis → compensatory erythrocytosis. Right shift:- ↑ H+, CO2, exercise- ↑ 2,3-BCG- ↑ Altitude- ↑ Temperature Fetal Hb has higher affinity to O2 (due to low affinity for 2,3-BPG), so its dissociation curve is shifted left.
• Response to high altitude - ↓ atmospheric oxygen (PO2) → ↓ PaO2 → ↑ ventilation → ↓ PaCO2 → respiratory alkalosis → altitude sickness. - Chronic ↑ in ventilation. - ↑ erythropoietin → ↑ hematocrit and Hb (due to chronic hypoxia)- ↑ 2,3-BPG (binds to Hb so that Hb releases more O2)- Cellular changes (↑ mitochondria)- ↑ renal excretion of HCO3- to compensate for respiratory alkalosis (can augment with acetazolamide) - Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.
• Rhinosinusitis Obstruction of sinus drainage into nasal cavity → inflammation and pain - Typically affects maxillary sinuses, which drain against gravity due to ostia located superomedially - Most common acute cause is viral URI; may lead to superimposed bacterial infection, most commonly S pneumoniae, H influenzae, M catarrhalis. - Infections in sphenoid or ethmoid sinuses may extend to caverous sinus and cause complications (eg, cavernous sinus syndrome).
• Epistaxis = Nose bleed Most commonly in anterior segment of nostril (Kiesselbach plexus):- Anterior and posterior ethymoidal arteries- Superior labial artery- Greater palatine artery- Sphenopalatine artery - Life-threatening hemorrhages in posterior segment (sphenopalatine artery, a branch of maxillary artery).  Common causes include foreign body, trauma, allergic rhinitis, and nasal angiofibromas (common in adolescent males).
• Head and neck cancer Mostly squamous cell carcinoma. Risk factors:- Tobacco- Alcohol- HPV-16 (oropharyngeal)- EBV (nasopharyngeal) Field cancerization: carcinogen damages wide mucosal area → multiple tumors that develop independently after exposure.
• Deep venous thrombosis Blood clot within deep vein → swelling, redness, warmth, pain. Predisposed by Virchow triad (SHE):- Stasis (eg, post-op, long drive/flight)- Hypercoagulability (eg, defect in coagulation cascade proteins, such as factor V Leiden, OCP use)- Endothelial damage (exposed collagen triggers clotting cascade) - Homan sign (dorsiflexion of foot) → calf pain- D-dimer lab used clinically to rule out DVT (high sensitivity, low specificity).- Imaging of choice is compression ultrasound with Doppler. - Most pulmonary emboli arise from proximal deep veins of lower extremity. - Use unfractionated heparin or LMWH (eg, enoxaparin) for prophylaxis and acute management.- Use oral anticoagulants (eg, warfarin, rivaroxaban) for treatment (long-term prevention).
• Pulmonary emboli V/Q mismatch, hypoxemia, respiratory alkalosis. - Sudden-onset dyspnea- Pleuritic chest pain- Tachypnea- Tachycardia- Large emboli or saddle embolus may cause sudden death due to electromechanical dissociation. - Lines of Zahn are interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death; help distinguish pre- and postmortem thrombi. Types: - Fat – associated with long bone fractures and liposuction; classic triad of hypoxemia, neurologic abnormalities, petechial rash- Air – nitrogen bubbles precipitate in ascending divers (caisson disease/decompression sickness); treat with hyperbaric O2; or, can be iatrogenic 2° to invasive procedures (eg, central line placement)- Thrombus- Bacteria- Amniotic fluid – can lead to DIC, especially postpartum- Tumor - CT pulmonary angiography is imaging test of choice- May have S1Q3T3 abnormality on ECG.
• Obstructive lung diseases Obstruction of air flow → air trapping in lungs. Airways close prematurely at high lung volumes → ↑ RV, ↑ FRC, ↑ TLC (→ barrel chest). Pulmonary flow tests: ↓↓ FEV1, ↓ FVC → ↓ FEV1/FVC ratio (forced vital capacity) = hallmark.V/Q mismatch. - Chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale. - Asthma- COPD (includes chronic bronchitis and emphysema)- Bronchiectasis
• Chronic bronchitis ("blue bloater") Obstructive lung diseaseDiagnostic criteria: productive cough for >3 months per year for >2 consecutive years. Findings:- Wheezing, crackles- Cyanosis (hypoxemia due to shunting)- Dyspnea- CO2 retention (hypercapnia)- 2° polycythemia Pathology: Hypertrophy and hyperplasia of mucus-secreting glands in bronchi → Reid index (thickness of mucosal gland layer to thickness of wall between epithelium and cartilage) > 50%.- DLCO usually normal. Chronic complications: Pulmonary hypertension, cor pulmonale
• Emphysema ("pink puffer") Obstructive lung diseaseEnlargement of air spaces, ↓ recoil, ↑ compliance, ↓ DLCO from destruction of alveolar walls.Imbalance of proteases and antiproteases → ↑ elastase activity → ↑ loss of elastic fibers → ↑ lung compliance. - Centriacinar – associated with smoking. Frequently in upper lobes (smoke rises up).- Panacinar – associated with α1-antitrypsin deficiency. Frequently in lower lobes. Findings:- Barrel-shaped chest- Exhalation through pursed lips (increases airway pressure and prevents airway collapse). - CXR: ↑ AP diameter, flattened diaphragm, ↑ lung field lucency
• Asthma Obstructive lung diseaseHyperresponsive bronchi → reversible bronchoconstriction. Type I hypersensitivity reaction.Triggers: viral URIs, allergens, stress. Findings: - Cough, wheezing- Tachypnea, dyspnea, hypoxemia- ↓ inspiratory/expiratory ratio- Pulsus paradoxus Pathology:- Smooth muscle hypertrophy and hyperplasia.- Curshmann spirals (shed epithilium forms whorled mucous plugs)- Charcot-Leyden crystals (eosinophilic, hexagonal, double-pointed needle-like crystals formed from breakdown of eosinophils in sputum)- DLCO normal or ↑. Diagnosis supported by spirometry and methacholine challenge. Aspirin-induced asthma is a combination of COX inhibition (leukotriene overproduction → airway constriction), chronic sinusitis with nasal polyps, and asthma symptoms.
• Bronchiectasis Obstructive lung diseaseChronic necrotizing infection of bronchi → permanently dilated airways. Findings:- Purulent sputum- Recurrent infections- Hemoptysis- Digital clubbing Associated with bronchial obstruction, poor ciliary motility (eg, Kartagener syndrome), cystic fibrosis, allergic bronchopulmonary aspergillosis.
• Asbestosis Pneumoconiosis Associated with shipbuilding, roofing, plumbing. (Asbestosis is from the roof, but affects the base) - "Ivory white," calcified, supradiaphragmatic and pleural plaques are pathognomonic. - Risk of bronchiogenic carcinoma > mesothelioma.- ↑ risk of pleural effusions. - Affects lower lobes.- Asbestos (ferruginous) bodies are golden-brown fusiform rods resembling dumbbells, found in alveolar sputum sample, visualized using Prussian blue stain, often obtained by bronchoalveolar lavage.- Restrictive ventilatory defects
• Silicosis Pneumoconiosis Associated with sandblasting, foundries, mines, glass production. - Macrophages respond to silica and release fibrogenic factors, leading to fibrosis.- It is thought that silica may disrupt phagolysosomes and impair macrophages, increasing susceptibility to TB. - ↑ risk of cancer, cor pulmonale, and Caplan syndrome. - Affects upper lobes.(Silica and coal are from the base, but affect the roof)- "Eggshell" calcification of hilar lymph nodes on CXR.
• Acute respiratory distress syndrome Alveolar insult → release of pro-inflamatory cytokines → neutrophil recruitment, activation, and release of toxic mediators (eg, reactive oxygen species, proteases, etc) → capillary endothelial damage and ↑ vessel permeability → leakage of protein-rich fluid into alveoli → formation of intra-alveolar hyaline membranes and noncardiogenic pulmonary edema (normal PCWP).- Loss of surfactant also contributes to alveolar collapse. Causes: Sepsis (most common), aspiration, pneumonia, trauma, pancreatitis, amniotic fluid embolism Diagnosis of exclusion with the following criteria:- Abnormal chest X-ray (bilateral lung opacities)- Respiratory failure within 1 week of alveolar insult- Decreased PaO2/FiO2 (ratio <300, hypoxemia due to ↑ intrapulmonary shunting and diffusion abnormalities)- Symptoms of respiratory failure are not due to HF/fluid overload Consequences: Impaired gas exchange, ↓ lung compliance, pulmonary hypertension Management with mechanical ventilation: ↓ tidal volumes, ↑ PEEP
• Sleep apnea Repeated cessation of breathing >10 seconds during sleep → disrupted sleep → daytime somnolence. Diagnosis confirmed by sleep study. Normal PaO2 during the day.Nocturnal hypoxia → systemic/pulmonary hypertension → arrhythmias (atrial fibrillation/flutter), sudden death.Hypoxia → ↑ EPO release → ↑ erythropoiesis. Obstructive sleep apnea: Respiratory effort against airway obstruction.- Associated with obesity, loud snoring, daytime sleepiness.- Cased by excess parapharyngeal tissue in adults, adenotonsillar hypertrophy in children.- Treatment: weight loss, CPAP, surgery. Central sleep apnea: Impaired respiratory effort due to CNS injury/toxicity, HF, opioids.- May be associated with Chyne-Stokes respirations (oscillations between apnea and hyperpnea).- Treat with positive airway pressure. Obesity hypoventilation syndrome:- Morbid obesity (BMI ≥30 kg/m2) → hypoventilation → ↑ PaCO2 during waking hours (retention); ↓ PaO2 and ↑ PaCO2 during sleep.- Also known as Pickwickian syndrome.
• Lung – physical findings Pleural effusion:- ↓ breath sounds- Dull percussion- ↓ fremitus Atelectasis (bronchial obstruction):- ↓ breath sounds- Dull percussion- ↓ fremitus- Tracheal deviation toward side of lesion Consolidation (lobar pneumonia, pulmonary edema):- Bronchial breath sounds; late inspiratory crackles, egophony, whispered pectoriloquy- Dull percussion- ↑ fremitus Pneumothorax- ↓ breath sounds- Hyperresonant percussion- ↓ fremitus- Tracheal deviation away from side of lesion (tension pneumothorax)
• Pleural effusions Excess accumulation of fluid between pleural layers → restricted lung expansion during inspiration. Can be treated with thoracocentesis to remove/reduce fluid. Transsudate: ↓ protein content.- Due to ↑ hydrostatic pressure (eg, HF), or ↓ oncotic pressure (eg, nephrotic syndrome, cirrhosis). Exudate: ↑ protein content, cloudy.- Due to malignancy, pneumonia, collagen vascular disease, trauma (occurs in states of ↑ vascular permeability).- Must be drained due to risk of infection. Lymphatic (chylothorax): Milky- Due to thoracic duct injury form trauma or malignancy.- ↑ triglycerides
• Pneumothorax Accumulation of air in pleural space. Dyspnea, uneven chest expansion. Chest pain, ↓ tactile fremitus, hyperresonance, and diminished breath sounds. Primary sponteanous pneumothorax: - Due to rupture of apical subpleural bleb or cysts.- Most frequently in tall, thin, young males and smokers. Secondary spontanous pneumothorax: - Due to diseased lung (eg, bullae in emphysema, infections), mechanical ventilation use of high pressures → barotrauma. Traumatic pneumothorax:- Caused by blunt (eg, rib fracture) or penetrating (eg, gunshot), or iatrogenic (eg, central line placement, lung biopsy, barotrauma due to mechanical ventilation) trauma. Tension pneumothorax: - Can be any of the above. Air enters pleural space but cannot exit → increasing trapped air.- Trachea deviates away from affected lung. - Needs immediate needle decompression and chest tube placement.- May lead to ↑ intrathoracic pressure → ↓ venous return → ↓ cardiac function.
• Pancoast tumor Carcinoma that occurs in the apex of lung. Compression of locoregional structures may cause array of findings:- Recurrent laryngeal nerve → hoarseness- Superior cervical ganglion (stellate ganglion) → Horner syndrome (ipsilateral ptosis, miosis, anhidrosis)- Superior vena cava → SVC syndrome- Brachiocephalic vein → brachiocephalic syndrome (unilateral symptoms)- Brachial plexus → sensorimotor deficits
• Superior vena cava syndrome An obstruction of the SVC that impairs blood drainage from the head. - Facial plethora- Jugular venous distension- Edema in upper extremities Commonly caused by malignancies (eg, mediastinal mass, Pancoast tumor) and thrombosis from indwelling catheters. Medical emergency. Can raise intracranial pressure → headaches, dizziness, ↑ risk of aneurysm/rupture of intracranial arteries.
• Small cell (oat cell) carcinoma Location: CentralUndifferentiated → very aggressive. - May produce ACTH (Cushing syndrome), SIADH, or antibodies against presynaptic Ca2+ channels (Lambert-Eaton myasthenic syndrome), or neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration). - Amplification of myc oncogenes common. Histology:- Neoplasm of neuroendocrine Kulchitsky cells → small dark blue cells- Chromogranin A ⊕, neuron-specific enolase ⊕, synpatophysin ⊕, neural cell adhesion molecule (NCAM/CD56) ⊕ Treatment: Chemotherapy +/- radiation
• Adenocarcinoma Location: Peripheral - Most common 1° lung cancer. - More common in women than men, most likely arise in nonsmokers.- Activating mutations include KRAS, EGFR, and ALK. - Associated with hypertorphic osteoarthropathy (clubbing). Bronchioloalveolar subtype (adenocarcinoma in situ): CXR often shows hazy infiltrates similar to pneumonia; better prognosis.Bronchial carcinoid and bronchioloalveolar cell carcinoma have lesser association with smoking. - Glandular pattern on histology, often stains mucin ⊕.- Bronchioloalveolar subtype: grows along alveolar septa → apparent "thickening" of alveolar walls. Tall, columnar cells containing mucus.
• Squamous cell carcinoma Location: Central - Hilar mass arising from bronchus- Cavitation- Cigarettes- Hypercalcemia (produces PTHrP) Histology: Keratin pearls and intracellular bridges.
• Large cell carcinoma Location: PeripheralHighly anaplastic undifferentiated tumor; poor prognosis. - Strong association with smoking. Histology: Pleomorphic giant cells Treatment: Less responsive to chemotherapy; removed surgically
• Lung development Occurs in five stages. Initial development includes development of lung bud from distal end of respiratory diverticulum during week 4. Embyronic (weeks 4-7): Lung bud → trachea → bronchial buds → mainstem bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi.- Errors at this stage can lead to tracheoesophageal fistula. Pseudoglandular (weeks 5-17): Endodermal tubules → terminal bronchioles.- Respiration impossible, incompatible with life. Canalicular (weeks 16-25): Terminal bronchioles → respiratory bronchioles → alveolar ducts. Surrounded by prominent capillary network.- Respiration capable at 25 weeks.- Pneumocytes develop starting at 20 weeks. Saccular (week 26-birth): Alveolar ducts → terminal sacs. Terminal sacs separated by 1° septae.  Alveolar (week 36-8 years): Terminal sacs → adult alveoli (due to 2° septation).- In utero, "breathing" occurs via aspiration and expulsion of amniotic fluid → ↑ vascular resistance through gestation. At birth, fluid gets replaced with air → ↓ in pulmonary vascular resistance.- At birth: 20-70 million alveoli.- By 8 years: 300-400 million alveoli.
• Congenital lung malformations Pulmonary hypoplasia: Poorly developed bronchial tree with abnormal histology. Associated with congenital diaphragmatic hernia (usually left-sided), bilateral renal agenesis (Potter sequence). Bronchiogenic cysts: Caused by abnormal budding of the foregut and dilation of terminal or large bronchi. Discrete, round, sharply defined, fluid-filled densities on CXR (air-filled if infected). Generally asymptomatic but can drain poorly, causing airway compression and/or recurrent respiratory infections.
• Club cells Nonciliated; low-columnar/cuboidal with secretory granules.  Located in bronchioles. Secrete component of surfactant; degrade toxins; act as reserve cells.
• Alveolar cell types Type I pneumocytes: - 97% of alveolar surfaces. Line the alveoli.- Squamous; thin for optimal gas diffusion. Type II pneumocytes:- Secrete surfactant from lamellar bodies → ↓ alveolar surface tension, prevents alveolar collapse, ↓ lung recoil, and ↑ compliance.- Cuboidal and clustered.- Also serve as precusors to type I cells and other type II cells. - Proliferate during lung damage. Collapsing pressure (P) = 2 x (surface tension)/radiusAlveoli have ↑ tendency to collapse on expiration as radius ↓ (law of Laplace).Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC). Surfactant synthesis begins around week 20 of gestation, but mature levels are not achieved until around week 35. Alveolar macrophages: Phagocytose foreign materials, release cytokines and alveolar proteases. Hemosiderin-laden macrophages may be seen in pulmonary hemorrhage.
• Lung relations Right lung has 3 lobes, Left lung has 2 lobes and lingula. Relation of the pulmonary artery to the bronchus at each lung hilium is described by RALS - Right Anterior; Left Superior. Right lung is more common side for inhaled foreign bodies because it is wider, more vertical and shorter.- Upright --> right lower lobe- Supine --> right upper lobe Fissure on posterior aspect of right and left lungs, dividing superior and inferior lobes = Oblique fissureFissue dividing right upper and middle lobe = Horizontal fissure
• Diaphragm structures Structures perforating diaphragm:- At T8: IVC, right phrenic nerve- At T10: Esophagus, vagus- At T12: Aorta, thoracic duct, azygos vein - Diaphragm is innervated by C3, 4, and 5 (phrenic nerve). - Pain from diaphragm irritation (eg, air, blood, or pus in peritoneal cavity) can be referred to shoulder (C5) and trapezius ridge (C3, 4). Other bifurcations:C4: Common carotid T4: TracheaL4: Abdominal aorta
• Lung volumes Note: A capacity is a sum of ≥2 physiologic volumes. Inspiratory reserve volume: Air that can still be breathed in after normal inspiration, typically 3.3 L.Tidal volume: Air that moves into lung with each quiet inspiration, typically 500 mL.Expiratory reserve volume: Air that can still be breathed out after normal expiration, typically 1 L.Residual volume: Air in lung after maximal expiration. RV cannot be measured by spirometry, typically 1.2 L. Inspiratory capacity: TV + IRV. Air that can be breathed in after normal exhalation.Functional residual capacity: ERV + RV. Volume of gas in lungs after normal expiration, typically 2.2 L.Vital capacity: TV + IRV + ERV. Maximum volume of gas that can be expired after a maximal inspiration.Total lung capacity: IRV + TV + ERV + RV. Volume of gas present in lungs after a maximal inspiration, typically 6 L.
• Hemoglobin modifications Methemoglobin:- Oxidized form of Hb (ferric, Fe3+) that does not bind O2 as readily as Fe2+, but has ↑ affinity for cyanide.- Iron in Hb is normally in a reduced state (ferrous, Fe2+).- Nitrates (eg, from dietary intake or polluted/high altitude water sources) and benzocaine cause poisoning by oxidizing Fe2+ to Fe3+.- Methemoglobinemia may present with cyanosis and chocolate-colored blood.- Methemoglobinemia can be treated with methylene blue and vitamin C.- Induced methemoglobinemia (using nitrates, followed by thiosulfate) may be used to treat cyanide poisoning. Carboxyhemoglobin:- Form of Hb bound to CO in place of O2.- Causes ↓ oxygen-binding capacity with left shift in oxygen-hemoglobin dissociation curve. ↓ O2 unloading in tissues.- CO binds competitively to Hb and with 200x greater affinity than O2.- CO poisoning can present with headaches, dizziness, and cherry red skin. May be caused by fires, car exhaust, or gas heaters.- Treat with 100% O2 and hyperbaric O2.
• Alveolar gas equation PAO2 = PIO2 - PaCO2/R ≈ 150 mmHg - PaCO2/0.8 PAO2 = alveolar PO2 (mmHg)PIO2 = PO2 in inspired air (mmHg)PaCO2 = arterial PCO2 (mmHg)R = respiratory quotient = CO2 produced/O2 consumed A-a gradient = PAO2 - PaO2. Normal range = 10-15 mmHg↑ A-a gradient may occur in hypoxemia; causes include shunting, V/Q mismatch, fibrosis (impairs diffusion).
• Oxygen deprivation Hypoxia (↓ O2 delivery to tissue)- ↓ cardiac output- Hypoxemia- Anemia- CO poisoning Hypoxemia (↓ PaO2)- Normal A-a gradient: High altitude, hypoventilation (eg, opioid use)- ↑ A-a gradient: V/Q mismatch, diffusion limitation (eg, fibrosis), right-to-left shunt Ischemia (loss of blood flow)- Impeded arterial flow- ↓ venous drainage
• Ventilation/perfusion mismatch Ideally, ventilation is matched to perfusion (ie, V/Q = 1) for adequate gas exchange. Lung zones:- V/Q at apex of lung = 3 (wasted ventilation)- V/Q at base of lung = 0.6 (wasted perfusion) Zone 1: PA > Pa > PvZone 2: Pa > PA > PvZone 3: Pa > Pv > PA Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung.With exercise (↑ cardiac output), there is vasodilation of apical capillaries → V/Q ratio approaches 1. V/Q = 0 = airway obstruction (shunt). In shunt, 100% O2 does not improve PaO2 (eg, foreign body aspiration),V/Q = ∞ = blood flow obstruction (physiologic dead space). Assuming <100% dead space, 100% O2 improves PaO2 (eg, pulmonary embolus).
• Carbon dioxide transport CO2 is transported from tissues to lungs in 3 forms:1. HCO3- (70%).2. Carbaminohemoglobin or HbCO2 (21-25%). CO2 bound to Hb at N-terminus of globin (not heme). CO2 binding favors deoxygenated form (O2 unloaded).3. Dissovled CO2 (5-9%). In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs (Haldane effect). In peripheral tissue, ↑ H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect).
• Flow volume loops Obstructive lung volumes > normal (↑ TLC, ↑ FRC, ↑ RV); restrictive lung volumes < normal. In obstructive, FEV1 is more dramatically reduced compared with FVC --> decreased FEV1/FVC ratio. In restrictive, FVC is more reduced or close to same compared with FEV1 --> increased or normal FEV1/FVC ratio.
• Restrictive lung diseases Restricted lung expansion causes ↓ lung volumes (↓ FVC and TLC).Pulmonary flow tests: ↑ FEV/FVC ratio. - Patients present with short, shallow breaths. Types:Poor breathing mechanics (extrapulmonary, peripheral hypoventilation, normal A-a gradient):- Poor muscular effort – polio, myasthenia gravis, Guillain-Barré syndrome- Poor structural apparatus – scoliosis, morbid obesityInterstitial lung diseases (pulmonary ↓ diffusing capacity, ↑ A-a gradient):- Pneumoconioses (eg, coal workers' pneumoconiosis, silicosis, asbestosis)- Sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma; ↑ ACE and Ca2+- Idiopathic pulmonary fibrosis (repeated cycles of lung injury and wound healing with ↑ collagen deposition, "honeycomb" lung appearance and digital clubbing)- Goodpasture syndrome- Granulomatosis with polyangiitis (Wegener)- Pulmonary Langerhans cell histiocytosis (eosinophlic granuloma)- Hypersensitivity pneumonitis- Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate) Hypersensitivity pneumonitis – mixed type III/IV hypersensitivity reaction to environmental antigen. Causes dyspnea, cough, chest tightness, headache. Often seen in farmers and those exposed to birds. Reversible in early stages if stimulus is avoided.
• Inhalation injury and sequelae Complication of smoke inhalation from fires or other noxious substances. - Caused by heat, particulates (<1 µm diameter), or irritants (eg, NH3) → chemical tracheobronchitis, edema, pneumonia, ARDS.- Many patients present 2° to burns, CO inhalation, cyanide poisoning, or arsenic poisoning. - Singed nasal hairs common on exam. - Bronchoscopy shows severe edema, congestion of bronchus, and soot deposition.
• Pneumoconiosis Coal workers' pneumoconiosis, silicosis and asbestosis → ↑ risk of cor pulmonale, cancer, and Caplan syndrome (rheumatoid arthritis and pneumoconiosis with intrapulmonary nodules). - Berylliosis, silicosis and coal workers' pneumoconiosis affect the upper lobes. - Asbestosis affects the lower lobes.
• Coal workers' pneumoconiosis Prolonged coal dust exposure → macrophages laden with carbon → inflammation and fibrosis.- Also known as black lung disease. - ↑ risk for Caplan syndrome (rheumatoid arthritis and pneumoconioses with intrapulmonary nodules).- Affects upper lobes.- Small (<1 cm), rounded nodular opacities seen on imaging. Anthracosis – asymptomatic condition found in many urban dwellers exposed to sooty air.
• Mesothelioma Malignancy of the pleura associated with asbestosis. Clinical findings:- Dyspnea and nonpleuritic chest pain- Fever, sweats, weight loss May result in hemorrhagic pleural effusion (exsudative), pleural thickening. - Psammoma bodies seen on histology- Long, slender microvilli and abundant tonofilaments- Cytokeratin and calretinin ⊕ in almost all mesotheliomas, ⊝ in most carcinomas.- Smoking not a risk factor.
• Pulmonary hypertension Normal mean pulmonary artery pressure = 10-14 mmHg.Pulmonary hypertension ≥25 mmHg at rest.- Results in arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries, plexiform lesions. Course: severe respiratory distress → cyanosis and RVH → death from decompensated cor pulmonale. Pulmonary arterial hypertension: - Idiopathic PAH- Hereditary PAH – often due to inactivating mutation in BMPR2 gene (normally inhibits vascular smooth muscle proliferation); poor prognosis. Pulmonary vascular endothelial dysfunction results in ↑ vasoconstrictors (eg, endothelin) and ↓ vasodilators (eg, NO and prostacyclins).- Other causes include drugs (eg, amphetamines, cocaine), connective tissue disease, HIV infection, portal hypertension, congenital heart disease, schistosomiasis. Left heart disease: Causes systolic/diastolic dysfunction and valvular disease. Lung diseases or hypoxia: Destruction of lung parenchyma (eg, COPD), lung inflammation/fibrosis (eg, interstitial lung diseases), hypoxemic vasoconstriction (eg, obstructive sleep apnea, living in high altitude). Chronic thromboembolic: Recurrent microthrombi → ↓ cross-sectional area of pulmonary vascular bed. Multifactorial: Causes include hematologic, systemic, and metabolic disorders, along with compression of the pulmonary vasculature by a tumor.
• Pneumonia Lobar:- S pneumoniae most frequently, also Legionella, Klebsiella.- Intra-alveolar exudate → consolidation; may involve entire lobe or the whole lung. Bronchopnemonia: - S pneumoniae, S aureus, H influenzae, Klebsiella.- Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving ≥1 lobe. Interstitial (atypical) pneumonia:- Mycoplasma, C pneumoniae, C psittaci, Legionella, viruses (RSV, CMV, influenza, adenovirus).- Diffuse patchy inflammation localized to interstitial areas at alveolar walls; diffuse distribution involving ≥1 lobe. Generally folllows a more indolent course ("walking" pneumonia). Cryptogenic organizing pneumonia (bronchiolitis obliterans organizing pneumonia [BOOP]):- Noninfectious pneumonia characterized by inflammation of bronchioles and surrounding structure. Etiology unknown. - Secondary organizing pneumonia caused by chronic inflammation diseases (eg, rheumatoid arthritis) or medication side effects (eg, amiodarone).- ⊝ sputum and blood cultures, no response to antibiotics. 4 weeks-18 years: Viral18-40 years: M pneumoniae, C pneumoniae40-65 years: S pneumoniae
• Natural history of lobar pneumonia Congestion:- Days 1-2- Red-purple, partial consolidation of parenchyma- Exudate with mostly bacteria Red hepatization:- Days 3-4- Red-brown, consolidated- Exudate with fibrin, bacteria, RBCs, WBCs Gray hepatization:- Days 5-7- Uniformly gray- Exudate full of WBCs, lysed RBCs, and fibrin Resolution:- Days 8+- Enzymes digest components of exudate
• Lung abscess Localized collection of pus within parenchyma. Caused by aspiration of oropharyngeal contents (especially in patients predisposed to loss of consciousness [eg, alcoholics, epileptics]), or bronchial obstruction (eg, cancer). - Due to anaerobes (eg, Bacteroides, Fusobacterium, Peptostreptococcus) or S aureus.- Lung abscess 2° to aspiration is most often found in right lung.  - Air-fluid levels often seen on CXR. - Fluid levels common in cavities; presence suggests cavitation. Treatment: Clindamycin

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